Collecting Duct Sodium Reabsorption in Deoxycorticosterone-Treated Rats

Haas, J. A.; Berndt, Theresa J.; Youngberg, Stephen P.; Knox, Franklyn G.

doi:10.1172/jci109291

Cited by 17 publications

(8 citation statements)

References 15 publications

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“…Furthermore, in wholekidney samples, there were significant increases in the protein abundance of two proximal Na transporters, NHE3 and NaPi-2 ( Table 2). Although these changes would predict increased proximal NaCl absorption, micropuncture studies have revealed that Na delivery to the early distal tubule is not decreased during aldosterone escape (11,12). These observations would suggest that any increases in proximal tubule reabsorption during aldosterone escape are compensated for by decreases in Na absorption in the loop of Henle.…”

Section: Figurementioning

confidence: 99%

The renal thiazide-sensitive Na-Cl cotransporter as mediator of the aldosterone-escape phenomenon

Wang¹,

Masilamani²,

Nielsen³

et al. 2001

J. Clin. Invest.

111

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Section: Figurementioning

confidence: 99%

The renal thiazide-sensitive Na-Cl cotransporter as mediator of the aldosterone-escape phenomenon

Wang¹,

Masilamani²,

Nielsen³

et al. 2001

J. Clin. Invest.

111

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“…13,25,26 This is associated with declining Na ϩ reabsorption in the distal nephron despite elevated levels of aldosterone and occurs independent of changes in GFR. 26,27 Indeed, early micropuncture measurements demonstrated increases in urine flow and Na ϩ delivery to the CD during escape. 26,27 Details about the specific site(s) along the distal nephron involved in decreased Na ϩ reabsorption during aldosterone escape and the exact transport proteins involved in this escape, though, largely remain obscure.…”

mentioning

confidence: 99%

Purinergic Inhibition of ENaC Produces Aldosterone Escape

Stockand

Mironova

Bugaj

et al. 2010

Journal of the American Society of Nephrology

110

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The mechanisms underlying "aldosterone escape," which refers to the excretion of sodium (Na ϩ ) during high Na ϩ intake despite inappropriately increased levels of mineralocorticoids, are incompletely understood. Because local purinergic tone in the aldosterone-sensitive distal nephron downregulates epithelial Na ϩ channel (ENaC) activity, we tested whether this mechanism mediates aldosterone escape. Here, urinary ATP concentration increased with dietary Na ϩ intake in mice. Physiologic concentrations of ATP decreased ENaC activity in a dosage-dependent manner. P2Y 2 Ϫ/Ϫ mice, which lack the purinergic receptor, had significantly less increased Na ϩ excretion than wild-type mice in response to high-Na ϩ intake. Exogenous deoxycorticosterone acetate and deletion of the P2Y 2 receptor each modestly increased the resistance of ENaC to changes in Na ϩ intake; together, they markedly increased resistance. Under the latter condition, ENaC could not respond to changes in Na ϩ intake. In contrast, as a result of aldosterone escape, wild-type mice had increased Na ϩ excretion in response to high-Na ϩ intake regardless of the presence of high deoxycorticosterone acetate. These data suggest that control of ENaC by purinergic signaling is necessary for aldosterone escape.

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“…In view of similar findings in other natriuretic conditions (8-10, 17, 23), it seems unlikely that medullary tonicity influenced reabsorption by this segment. In previous studies of segmental sodium transport during more massive volume expansion, we (10,17) and others (8,9,23) found net addition of sodium between the LDT of superficial nephrons and the papillary base, indicative of preferential inhibition of sodium reabsorption in juxtamedullary nephrons. Using pharmacologic manipulation of transport, we suggested that this inhibition was localized to the thin ascending limb of the LH (10).…”

Section: Discussionmentioning

confidence: 49%

Effect of Medullary Tonicity on Urinary Sodium Excretion in the Rat

Reineck¹,

Parma²

1982

J. Clin. Invest.

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A B S T R A C T In previous reports from this laboratory we have suggested that a reduction in medullary tonicity decreases the thin ascending loop of Henle sodium reabsorption and is in part responsible for the magnitude for the natriuresis accompanying 10% body weight Ringer loading. According to this postulate, one would expect that the medullary washout associated with water diuresis would also result in a natriuresis, but this does not occur. It is possible, however, that increased delivery from the proximal tubule is necessary to demonstrate an effect of medullary tonicity on urinary sodium excretion. Micropuncture studies were designed to test that possibility by increasing distal delivery by 2% Ringer loading in animals with and without reduced medullary tonicity. In an initial series of experiments the a-adrenergic agonist clonidine was used to induce a water diuresis. When given alone, this agent caused a marked decrease in urine osmolality and an increase in urine flow rate but had no effect on proximal reabsorption in either superficial or juxtamedullary nephrons, and did not alter urinary sodium excretion. Volume expansion with 2% body weight Ringer solution resulted in a significant fall in proximal reabsorption and a trivial increment in sodium excretion. When this same degree of volume expansion was conferred on animals undergoing a water diuresis, a marked increase in absolute and fractional sodium excretion occurred. In a second group of studies medullary tonicity was reduced in the left kidney only by removal of the left ureter 1 h before micropuncture. When these animals were infused with 2% body weight Ringer solution, proximal reabsorption was decreased in juxtamedullary nephrons, and a marked increase in sodium excretion was observed only from the left kidney. Finally, the effect of water diuresis on fractional sodium delivery to the early and late distal tubule of superficial nephrons during 2% Ringer loading was evaluated. Delivery to both of these sites was comparable after 2% Ringer loading alone and during 2% Ringer loading plus water diuresis.From these data, we conclude that medullary tonicity does influence renal sodium handling but that this effect is manifest in the final urine only under conditions in which proximal reabsorption is decreased. The data also suggest that this effect is limited to juxtamedullary nephrons and is probably localized to the thin ascending limb of the loop of Henle.

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Collecting Duct Sodium Reabsorption in Deoxycorticosterone-Treated Rats

Cited by 17 publications

References 15 publications

The renal thiazide-sensitive Na-Cl cotransporter as mediator of the aldosterone-escape phenomenon

The renal thiazide-sensitive Na-Cl cotransporter as mediator of the aldosterone-escape phenomenon

Purinergic Inhibition of ENaC Produces Aldosterone Escape

Effect of Medullary Tonicity on Urinary Sodium Excretion in the Rat

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